Transgenic mice (3xTg strain), with an overexpression of the amyloid precursor protein and Tau protein (two proteins associated with Alzheimer's disease), that develop cognitive deficits at 6 months of age were used as an Alzheimer's disease model.
The following groups were used (n=6 mice, respectively): 1) exposure of transgenic mice to the magnetic field, 2) sham exposure of transgenic mice, 3) exposure of non-transgenic mice (129/C57BL/6 strain), 4) sham exposure of non-transgenic mice.
Exposure duration: 20 hours/day for 3 months
|Exposure duration||20 hours/day for 3 months|
|Chamber||room without additional electronic devices (e.g. computers) and no lamps in close proximity to the exposure system|
|Setup||there were five layers in the exposure device (200 cm x 70 cm x 200 cm); inside the exposure device, there was a plastic rack (140 cm x 70 cm x 200 cm) with four floors; two beams of bronze wires oriented in the same direction (current direction) created a uniform magnetic field and were affixed tightly to the framework to decrease vibration and noise; when the system was on, the sound and temperature generated were similar to those of the normal environmental values|
|Sham exposure||A sham exposure was conducted.|
|Additional info||for sham exposure, the two wire beams of the setup were oriented in opposite directions|
|magnetic flux density||500 µT||-||measured||-||-|
The functionality of the Alzheimer's disease model was confirmed by significant cognitive deficits, significantly decreased gene expression of memory-related synaptic proteins as well as significantly increased apoptosis, oxidative stress and levels of total and phosphorylated Tau protein in sham exposed transgenic mice (group 2) compared to sham exposed non-transgenic mice (group 4).
Exposed transgenic mice (group 1) showed significantly better cognitive skills and a significantly increased gene expression of some memory-related synaptic proteins (GLUR2, NR1, PSD95) as well as significantly less apoptosis and oxidative stress compared to the transgenic sham exposure group.
Exposed transgenic mice also showed significantly less total and phosphorylated Tau protein compared to the transgenic sham exposure group. This decrease was accompanied by a significant decrease of phosphorylated GSK3β (inactive form) CDK5 activators p25 and p35 and a significant increase of PP2Ac, indicating that effects of the magnetic field exposure may be caused by inhibition of GSK3β and CDK5 and activation of PP2Ac.
Exposure to the magnetic field had no significant effect on non-transgenic mice (group 3) compared to sham exposed non-transgenic mice.
The authors conclude that exposure of Alzheimer's disease model mice to a 50 Hz magnetic field might ameliorate cognitive deficits and attenuate tau hyperphosphorylation. This might be of use in the therapy of Alzheimer's disease.